Diuretics Practice Questions

Q: A 72-year-old woman with mild heart failure is treated overzealously with a thiazide diuretic. A few days later, the woman complains of muscle weakness, and laboratory tests demonstrate hypokalemia. Which of the following is most likely increased in this woman?

Plasma aldosterone. **Explanation:** The correct answer is **B. Plasma aldosterone**. **Mechanism of Action:** Thiazide diuretics inhibit the $Na^+/Cl^-$ symporter in the distal convoluted tubule, leading to increased excretion of sodium and water. Overzealous use causes **volume depletion** (hypovolemia). This reduction in effective circulating volume triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. Juxtaglomerular cells sense decreased renal perfusion and release renin, ultimately leading to elevated levels of **Aldosterone**. Aldosterone then acts on the collecting ducts to reabsorb sodium at the expense of secreting potassium and hydrogen ions, which explains the patient's hypokalemia and muscle weakness. **Analysis of Incorrect Options:** * **A. Serum $H^+$ concentration:** Thiazides cause **metabolic alkalosis** (contraction alkalosis and increased $H^+$ secretion in the collecting duct). Therefore, $H^+$ concentration decreases, and pH increases. * **C. Plasma sodium:** Thiazides are a common cause of **hyponatremia**. They promote sodium excretion while the compensatory ADH release (due to volume depletion) causes water retention, diluting serum sodium. * **D. Potassium retention:** Thiazides cause **potassium wasting** (hypokalemia) due to increased sodium delivery to the late distal tubule and high aldosterone levels, both of which drive $K^+$ secretion. **NEET-PG High-Yield Pearls:** * **Thiazide Side Effects (Hyper-GLUC):** Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, and Hyper**C**alcemia. * **Electrolyte Profile:** Hypokalemic metabolic alkalosis + Hyponatremia. * **Clinical Note:** Unlike Loop diuretics (which cause hypocalcemia), Thiazides decrease urinary calcium and are used in treating **calcium nephrolithiasis**.

Q: A 55-year-old man with congestive heart failure is noted to be taking furosemide each day. Which of the following is most likely to be found in the serum?

Decreased potassium level. **Explanation:** **Mechanism of Action (The Correct Answer):** Furosemide is a high-ceiling **loop diuretic** that inhibits the **Na+/K+/2Cl- symporter** in the Thick Ascending Limb (TAL) of the Henle’s loop. By blocking this transporter, it increases the delivery of sodium to the distal convoluted tubule and collecting duct. In the collecting duct, the increased sodium load promotes sodium reabsorption in exchange for **potassium (K+) and hydrogen (H+) ions** via the action of aldosterone. This leads to increased urinary excretion of potassium, resulting in **hypokalemia** (decreased serum potassium levels). **Analysis of Incorrect Options:** * **A. Decreased uric acid level:** Incorrect. Loop diuretics cause **hyperuricemia** (elevated uric acid). This occurs because diuretics cause volume depletion, leading to increased proximal tubular reabsorption of uric acid, and they compete with uric acid for the organic acid secretory pathway in the kidney. * **B. Low bicarbonate level:** Incorrect. Furosemide causes **contraction alkalosis**, which is characterized by an **increase** in serum bicarbonate levels due to the loss of H+ ions and volume contraction. * **D. Elevated magnesium level:** Incorrect. The Na+/K+/2Cl- symporter normally creates a positive lumen potential that drives the paracellular reabsorption of divalent cations. By inhibiting this, furosemide causes **hypomagnesemia** and **hypocalcemia**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Loop Diuretic Side Effects:** "OH DANG!" (**O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (sulfa), **N**ephritis, **G**out). * **Calcium Handling:** Unlike Thiazides (which cause hypercalcemia), Loop diuretics cause **hypocalcemia** ("Loops Lose Calcium"). * **Drug of Choice:** Furosemide is the drug of choice for acute pulmonary edema in CHF due to its rapid-acting diuretic and vasodilator properties.

Q: Dorzolamide is a:

Topically applied ocular carbonic anhydrase inhibitor. **Explanation:** **Dorzolamide** is a potent, highly specific inhibitor of the enzyme **Carbonic Anhydrase (Type II)**. In the eye, carbonic anhydrase is essential for the production of aqueous humor by the ciliary body epithelium. By inhibiting this enzyme, Dorzolamide reduces the secretion of aqueous humor, thereby lowering intraocular pressure (IOP). It is specifically designed for **topical application** as an ophthalmic solution to avoid the systemic side effects (like metabolic acidosis or electrolyte imbalance) associated with oral carbonic anhydrase inhibitors like Acetazolamide. **Analysis of Incorrect Options:** * **Option A:** Second-generation sulfonylureas (e.g., Glibenclamide, Glipizide) are used for Type 2 Diabetes. While Dorzolamide shares a sulfonamide structure, it has no hypoglycemic activity. * **Option B:** Although Dorzolamide is a sulfonamide derivative, it lacks clinically significant antimicrobial activity. Topical sulfonamide antibacterials include drugs like Sulfacetamide. * **Option C:** Luminal amoebicides (e.g., Diloxanide furoate, Iodoquinol) act within the bowel lumen to treat intestinal amoebiasis; they are unrelated to carbonic anhydrase inhibition. **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Primarily used in Open-Angle Glaucoma and Ocular Hypertension. * **Side Effects:** The most common side effect is a **bitter taste (dysgeusia)** following application due to drainage through the nasolacrimal duct. It can also cause local stinging and superficial punctate keratitis. * **Contraindication:** Avoid in patients with known **sulfonamide hypersensitivity**. * **Brinzolamide** is another topical carbonic anhydrase inhibitor; it is often preferred over Dorzolamide as it causes less ocular stinging.

Q: Which of the following statements about diuretics is NOT true?

Acetazolamide is a carbonic anhydrase stimulant.. ### Explanation **1. Why Option A is the Correct Answer (The "Not True" Statement):** Acetazolamide is a **Carbonic Anhydrase (CA) Inhibitor**, not a stimulant. It works in the proximal convoluted tubule (PCT) by inhibiting the enzyme carbonic anhydrase. This prevents the dehydration of carbonic acid and the reabsorption of bicarbonate ($HCO_3^-$), leading to alkaline diuresis. Because it inhibits the enzyme, the statement claiming it is a "stimulant" is factually incorrect. **2. Analysis of Other Options:** * **Option B (Thiazides):** This is **true**. Thiazides act on the early distal convoluted tubule (DCT), which is also known as the **cortical diluting segment**. They inhibit the $Na^+-Cl^-$ symporter. * **Option C (Furosemide):** This is **true**. Furosemide is a loop diuretic that acts on the thick ascending limb of Henle. It is called "high-ceiling" because it has a steep dose-response curve, meaning increasing the dose leads to a proportional increase in diuresis over a wide range. * **Option D (Spironolactone):** This is **true**. It is a potassium-sparing diuretic that competitively inhibits the **aldosterone receptor** (Mineralocorticoid receptor) in the late DCT and collecting ducts. **3. NEET-PG High-Yield Clinical Pearls:** * **Acetazolamide Uses:** Glaucoma (decreases aqueous humor), Mountain sickness (induces metabolic acidosis to stimulate respiration), and Urinary alkalization. * **Side Effects:** Metabolic acidosis, hypokalemia, and sulfonamide-like hypersensitivity. * **Thiazide Paradox:** While they are diuretics, they are used to treat **Diabetes Insipidus** because they reduce glomerular filtration and increase proximal salt/water reabsorption. * **Furosemide Side Effects:** Remember the mnemonic **OH DANG**: **O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (sulfa), **N**ephritis, **G**out (hyperuricemia).

Q: All of the following diuretics inhibit the Na+-K+-2Cl- symporter, except?

Thiazide. The question tests the knowledge of the site of action and molecular targets of various diuretics. 1. Why Thiazide is the Correct Answer: Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) act on the **Distal Convoluted Tubule (DCT)** [1]. Their primary mechanism is the inhibition of the **Na+-Cl- symporter** (NCC) on the luminal membrane [1, 3]. They do not affect the Na+-K+-2Cl- (NKCC2) transporter [3]. 2. Analysis of Incorrect Options (Loop Diuretics): The other three options belong to the class of **Loop Diuretics**, which specifically inhibit the **Na+-K+-2Cl- (NKCC2) symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle [2, 4]: * **Furosemide:** A prototype high-ceiling loop diuretic (Sulfonamide derivative). * **Ethacrynic acid:** A phenoxyacetic acid derivative. It is a non-sulfonamide loop diuretic, making it the drug of choice for patients with sulfonamide allergies. * **Mersalyl:** An older organomercurial diuretic that also acts on the TAL to inhibit the same symporter, though it is now obsolete due to toxicity. Clinical Pearls for NEET-PG: * **Site of Action:** Loop diuretics act on the TAL (medullary and cortical), while Thiazides act on the cortical DCT. * **Calcium Handling:** This is a high-yield differentiator. Loop diuretics cause **Hypercalciuria** (used in treating hypercalcemia), whereas Thiazides cause **Hypocalciuria** (used in treating calcium nephrolithiasis). * **Ototoxicity:** Ethacrynic acid is the most ototoxic loop diuretic. * **Metabolic Side Effects:** Both classes can cause hypokalemia and metabolic alkalosis.

Q: Which of the following antihypertensive agents is contraindicated in patients with chronic renal disease?

Hydrochlorothiazide-triamterene. **Explanation:** The correct answer is **A. Hydrochlorothiazide-triamterene**. **Why it is correct:** This combination contains **Triamterene**, a potassium-sparing diuretic. In chronic renal disease (CRD), the kidneys' ability to excrete potassium is significantly impaired. Using potassium-sparing agents like triamterene, amiloride, or spironolactone in these patients poses a high risk of life-threatening **hyperkalemia**. Furthermore, **Thiazides** (like Hydrochlorothiazide) lose their efficacy as monotherapy when the Glomerular Filtration Rate (GFR) falls below 30 mL/min, making this combination both dangerous and ineffective in advanced renal failure. **Why the other options are incorrect:** * **B. Furosemide:** This is a loop diuretic and is the **diuretic of choice** in patients with renal impairment. Unlike thiazides, loop diuretics remain effective even at low GFR levels and help manage fluid overload in CRD. * **C. Prazosin:** This is an alpha-1 blocker. It is primarily metabolized by the liver and does not require significant dose adjustment in renal failure, making it safe for use. * **D. Nifedipine:** This is a Calcium Channel Blocker (CCB). CCBs are generally safe in renal disease as they do not adversely affect renal hemodynamics and are often used to manage hypertension in these patients. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperkalemia Risk:** Always avoid the "K-SPARE" drugs (Spironolactone, Amiloride, Triamterene) and ACE inhibitors/ARBs in patients with advanced renal failure or high baseline potassium. * **Thiazide Limit:** Thiazides are generally ineffective if **CrCl < 30 mL/min** (Exception: Metolazone). * **Drug of Choice:** Loop diuretics (Furosemide) are preferred for edema/hypertension in renal insufficiency.

Q: Furosemide is useful in:

Refractory oedema.. **Explanation:** **1. Why "Refractory Oedema" is correct:** Furosemide is a potent **Loop Diuretic** that acts by inhibiting the **Na⁺-K⁺-2Cl⁻ symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle. It is known as a "high-ceiling" diuretic because it has a steep dose-response curve; increasing the dose leads to a progressive increase in diuresis. This makes it the drug of choice for **refractory oedema** (oedema not responding to milder diuretics) associated with Congestive Heart Failure, Nephrotic Syndrome, and Chronic Renal Failure. **2. Why other options are incorrect:** * **A. Hypertension:** While loop diuretics can be used in hypertension complicated by renal failure, **Thiazides** are the first-line diuretic for essential hypertension due to their longer duration of action and vasodilator properties. * **C. Hypocalcemia:** Furosemide increases the urinary excretion of calcium ("Loop loses Calcium"). Therefore, it is used to treat **Hypercalcemia**, not hypocalcemia. * **D. Hypokalemia:** Furosemide causes significant potassium loss in the urine. It is a *cause* of hypokalemia, not a treatment for it. **3. High-Yield NEET-PG Pearls:** * **Mechanism:** Inhibits Na⁺-K⁺-2Cl⁻ (NKCC2) in the TAL. * **Electrolyte Profile:** Causes Hypokalemia, Hypomagnesemia, and **Hypocalcemia**. * **Ototoxicity:** This is a unique side effect of loop diuretics, especially when used with aminoglycosides. * **Acute Pulmonary Oedema:** Furosemide is the drug of choice here, not just for its diuretic effect, but for its rapid **venodilatory action** (mediated by prostaglandins), which reduces cardiac preload.

Q: Hyperkalemia is caused by all EXCEPT:

Loop diuretics. ### Explanation The correct answer is **Loop diuretics** because they cause **hypokalemia** (low potassium), not hyperkalemia. #### 1. Why Loop Diuretics (Option A) are the Correct Answer: Loop diuretics (e.g., Furosemide) inhibit the **Na⁺-K⁺-2Cl⁻ symporter** in the Thick Ascending Limb of the Loop of Henle. This leads to a massive delivery of sodium to the distal tubule. To reabsorb this sodium, the distal tubule activates the Na⁺/K⁺ exchange mechanism (driven by aldosterone), which results in the **excretion of potassium** into the urine. This process, combined with volume depletion-induced secondary hyperaldosteronism, leads to hypokalemia. #### 2. Why the other options are incorrect (They cause Hyperkalemia): * **Amiloride (Option C):** This is a potassium-sparing diuretic that blocks the **ENaC (Epithelial Sodium Channels)** in the collecting duct. By preventing sodium reabsorption, it reduces the negative luminal potential, thereby inhibiting the secretion of potassium into the lumen. * **Enalapril (Option D) & Valsartan (Option B):** Enalapril (an ACE inhibitor) and Valsartan (an ARB) both interfere with the **Renin-Angiotensin-Aldosterone System (RAAS)**. By decreasing aldosterone levels or blocking its action, they prevent potassium excretion in the distal nephron, leading to potassium retention. #### 3. NEET-PG High-Yield Pearls: * **Diuretics causing Hypokalemia:** Loop diuretics and Thiazides. * **Diuretics causing Hyperkalemia:** Spironolactone, Eplerenone (Aldosterone antagonists), Amiloride, and Triamterene. * **Clinical Tip:** Always monitor serum potassium when combining ACE inhibitors with potassium-sparing diuretics, as this significantly increases the risk of life-threatening hyperkalemia. * **ECG in Hyperkalemia:** Look for "Tall tented T-waves" and "Widened QRS complex."

Q: Which drug is used in the treatment of idiopathic hypercalciuria?

Thiazide. ### Explanation **Correct Option: D (Thiazide)** Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) are the drugs of choice for idiopathic hypercalciuria. * **Mechanism:** Thiazides inhibit the $Na^+/Cl^-$ symporter in the Distal Convoluted Tubule (DCT). This decrease in intracellular sodium enhances the activity of the $Na^+/Ca^{2+}$ exchanger on the basolateral membrane, which pumps $Na^+$ into the cell and $Ca^{2+}$ out into the blood. * **Result:** This leads to increased reabsorption of calcium from the tubular fluid, thereby **decreasing urinary calcium excretion** (hypocalciuria). By lowering the concentration of calcium in the urine, Thiazides prevent the formation of calcium oxalate stones. **Analysis of Incorrect Options:** * **A. Allopurinol:** A xanthine oxidase inhibitor used for hyperuricemia and uric acid stones, but it does not directly affect renal calcium handling. * **B. Furosemide:** A loop diuretic that inhibits the $Na^+/K^+/2Cl^-$ cotransporter. It **increases** urinary calcium excretion ("Loops Lose Calcium") and is actually used to treat hypercalcemia. It would worsen hypercalciuria. * **C. Acetazolamide:** A carbonic anhydrase inhibitor. It increases urinary bicarbonate and can lead to alkaline urine, which actually promotes the precipitation of calcium phosphate stones. **NEET-PG High-Yield Pearls:** * **Mnemonic:** "Loops Lose calcium, Thiazides Thank (retain) calcium." * **Clinical Use:** Thiazides are unique because they are the only diuretics that cause **hypocalciuria**. * **Side Effects:** Remember the "4 Hypers" of Thiazides: Hyperglycemia, Hyperlipidemia, Hyperuricemia, and **Hypercalcemia**. * **Drug of Choice:** For Nephrogenic Diabetes Insipidus, Thiazides are also the preferred treatment.

Q: Paradoxical action is seen with which of the following diuretics?

Thiazide. **Explanation:** The "paradoxical action" of **Thiazide diuretics** refers to their ability to **reduce urine volume** in patients with **Diabetes Insipidus (DI)**, despite being diuretics that normally increase urine output in healthy individuals. **Mechanism of Paradoxical Action:** In Diabetes Insipidus, there is a deficiency or resistance to ADH, leading to the excretion of large volumes of dilute urine. Thiazides inhibit the Na⁺-Cl⁻ symporter in the distal convoluted tubule, causing mild natriuresis. This leads to a slight depletion of total body sodium and a decrease in extracellular fluid (ECF) volume. In response, the proximal tubule increases the reabsorption of water and sodium to compensate. Consequently, less fluid reaches the distal parts of the nephron, resulting in a net reduction in final urine volume. **Analysis of Incorrect Options:** * **B & C (Triamterene & Spironolactone):** These are potassium-sparing diuretics. While they act on the late distal tubule and collecting duct, they do not exhibit this specific paradoxical effect in DI. * **D (Furosemide):** This is a potent loop diuretic. It is contraindicated in DI because it interferes with the medullary osmotic gradient, further impairing the kidney's ability to concentrate urine and potentially worsening dehydration. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Thiazides (specifically Chlorthalidone or Hydrochlorothiazide) are the treatment of choice for **Nephrogenic Diabetes Insipidus**. * **Electrolyte Side Effects:** Remember the "4 Hypo, 2 Hyper" rule for Thiazides: **Hypo**kalemia, **Hypo**natremia, **Hypo**magnesemia, **Hypo**chloremic alkalosis; **Hyper**uricemia, and **Hyper**calcemia (unlike Loop diuretics which cause hypocalcemia). * **Lithium-Induced DI:** Amiloride is the preferred agent for DI specifically caused by Lithium toxicity.

Question 1

A 72-year-old woman with mild heart failure is treated overzealously with a thiazide diuretic. A few days later, the woman complains of muscle weakness, and laboratory tests demonstrate hypokalemia. Which of the following is most likely increased in this woman?

Accepted Answer

Plasma aldosterone

Answer

Serum H+ concentration

Answer

Plasma sodium

Answer

Potassium retention

Question 2

A 55-year-old man with congestive heart failure is noted to be taking furosemide each day. Which of the following is most likely to be found in the serum?

Accepted Answer

Decreased potassium level

Answer

Decreased uric acid level

Answer

Low bicarbonate level

Answer

Elevated magnesium level

Question 3

Dorzolamide is a:

Accepted Answer

Topically applied ocular carbonic anhydrase inhibitor

Answer

Second generation sulfonylurea hypoglycaemic

Answer

Topical sulfonamide antibacterial

Answer

Luminal amoebicide

Question 4

Which of the following statements about diuretics is NOT true?

Accepted Answer

Acetazolamide is a carbonic anhydrase stimulant.

Answer

Thiazides act on the cortical diluting segment of the nephron.

Answer

Furosemide is a high-ceiling diuretic.

Answer

Spironolactone is an aldosterone antagonist.

Question 5

All of the following diuretics inhibit the Na+-K+-2Cl- symporter, except?

Accepted Answer

Thiazide

Answer

Furosemide

Answer

Ethacrynic acid

Answer

Mersalyl

Question 6

Which of the following antihypertensive agents is contraindicated in patients with chronic renal disease?

Accepted Answer

Hydrochlorothiazide-triamterene

Answer

Furosemide

Answer

Prazosin

Answer

Nifedipine

Question 7

Furosemide is useful in:

Accepted Answer

Refractory oedema.

Answer

Hypertension.

Answer

Hypocalcemia.

Answer

Hypokalemia.

Question 8

Hyperkalemia is caused by all EXCEPT:

Accepted Answer

Loop diuretics

Answer

Valsartan

Answer

Amiloride

Answer

Enalapril

Question 9

Which drug is used in the treatment of idiopathic hypercalciuria?

Accepted Answer

Thiazide

Answer

Allopurinol

Answer

Furosemide

Answer

Acetazolamide

Question 10

Paradoxical action is seen with which of the following diuretics?

Accepted Answer

Thiazide

Answer

Triamterene

Answer

Spironolactone

Answer

Furosemide

Diuretics — MCQs

Diuretics — MCQs

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